Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Molecular and neuronal substrate for the selective attenuation of anxiety.

Science (New York, N.Y.) | Oct 6, 2000

http://www.ncbi.nlm.nih.gov/pubmed/11021797

Benzodiazepine tranquilizers are used in the treatment of anxiety disorders. To identify the molecular and neuronal target mediating the anxiolytic action of benzodiazepines, we generated and analyzed two mouse lines in which the alpha2 or alpha3 GABAA (gamma-aminobutyric acid type A) receptors, respectively, were rendered insensitive to diazepam by a knock-in point mutation. The anxiolytic action of diazepam was absent in mice with the alpha2(H101R) point mutation but present in mice with the alpha3(H126R) point mutation. These findings indicate that the anxiolytic effect of benzodiazepine drugs is mediated by alpha2 GABAA receptors, which are largely expressed in the limbic system, but not by alpha3 GABAA receptors, which predominate in the reticular activating system.

Pubmed ID: 11021797 RIS Download

Mesh terms: Animals | Anti-Anxiety Agents | Behavior, Animal | Binding Sites | Brain | Cells, Cultured | Diazepam | Dose-Response Relationship, Drug | Female | Gene Targeting | Hippocampus | Membrane Potentials | Mice | Patch-Clamp Techniques | Phenobarbital | Point Mutation | Pyramidal Cells | Receptors, GABA-A | Synaptic Transmission | gamma-Aminobutyric Acid

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

None

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.